Mornsett (2010) and include reductions of a barium-sensitive potassium and M-type currents. Furthermore, GIRK channels (Herman et al., 2015) and the hyperpolarization-activated and cyclic nucleotide-gated (HCN) channel current (Ih) (Appel et al., 2003; McDaid et al., 2008; Nimitvilai et al., 2016b) may also be involved in ethanol stimulation of dopamine neuron firing. Synaptic mechanisms also contribute to this stimulatory ethanol effect. Opioid (Xiao and Ye, 2008; Xiao et al., 2007), GABA, cholinergic, and serotoninergic transmission modulate ethanol excitation of VTA dopamine neurons (Adermark et al., 2014; Theile et al., 2009, 2011; Xiao and Ye, 2008; Xiao et al., 2007; but see Nimitvilai et al., 2016b) (Figures 2A and 2B). It is now clear that dopamine neurons are heterogeneous, and recent reports have identified a subset of VTA dopamine neurons with greater sensitivity to ethanol’s effects (Avegno et al., 2016; Mrejeru et al., 2015; Tateno and Robinson, 2011) (Figures 2A and 2D). The chronic and withdrawal effects of ethanol on dopamine neuron firing are mixed, with decreases observed in anesthetized rats (Diana et al., 1996) but no change (Okamoto et al., 2006; Perra et al., 2011) or increases (Didone et al., 2016) detected in slices. Repeated in vivo ethanol downregulates Ih
